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Gonadal gap junctions activate Notch signaling to suppress intestinal innate immunity via p38/PMK-1 and lysosome pathway II

ABSTRACT: Gonadal gap junctions activate Notch signaling to suppress intestinal innate immunity via p38/PMK-1 and lysosome pathway II

PROVIDER: PRJNA849251 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19658600_1.fastq.gz	Fastqsanger.gz
	SRR19658600_2.fastq.gz	Fastqsanger.gz
	SRR19658601_1.fastq.gz	Fastqsanger.gz
	SRR19658601_2.fastq.gz	Fastqsanger.gz
	SRR19658602_1.fastq.gz	Fastqsanger.gz

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Gonadal gap junctions activate Notch signaling to suppress intestinal innate immunity via p38/PMK-1 and lysosome pathway II

Project description:We showed that the innexin genes encoding gap junction subunits positively regulated GLP-1/Notch signaling to suppress the innate immunity of C. elegans via PMK-1/p38 pathway.

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Gonadal gap junctions activate Notch signaling to suppress intestinal innate immunity via p38/PMK-1 and lysosome pathway

Project description:We showed that the innexin genes encoding gap junction subunits positively regulated GLP-1/Notch signaling to suppress the innate immunity of C. elegans via PMK-1/p38 pathway. The unc-17 acts in the dowmstream of inx-14/glp-1 to regulate innate immunity.

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Gonadal gap junctions activate Notch signaling to suppress intestinal innate immunity via p38/PMK-1 and lysosome pathway

Project description:Gonadal gap junctions activate Notch signaling to suppress intestinal innate immunity via p38/PMK-1 and lysosome pathway

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Neuronal Acetylcholine Couples Gonadal Gap Junction/Notch Signaling Axis to Gut Defense

Project description:Gap junctions mediate intercellular communications across cellular networks in the nervous and the immune systems, while the role in the intestinal innate immunity is poorly understood. Here, we identified that an innexin gene inx-14 encoding one of heterotypic and heteromeric gap junction subunits acts in the gonad to attenuate the intestinal defense through PMK-1/p38 pathway. The RNA-seq analyses revealed that GLP-1/Notch signaling was downregulated, while lysosome, and PMK-1/p38 MAPK signalings were upregulated by the germline-specific inx-14 RNAi in C. elegans. Loss function of either inx-14, or glp-1 exhibited enhanced resistance to PA14 infection and upregulated lysosome and PMK-1/p38 signalings. Additionally, inx-14 knockdown by germline specific RNAi upregulated muscarinic acetylcholine receptor (mAChR) genes gar-1/gar-2/gar-3. We further revealed that acetylcholine mAChR GAR-2/GAR-3 signaling functions in the intestine and downstream of lysosome signaling but upstream of PMK-1/p38 pathway to facilitate the intestinal defense. Our findings reveal a novel role for gonadal gap junction/INX-14 in host intestinal defense against pathogens and expand our understanding the functions of reproductive system in the host intestinal defense.

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